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The Local Inflammatory Responses to Infection of the Peritoneal Cavity in Humans: Their Regulation by Cytokines, Macrophages, and Other Leukocytes

机译:人类感染腹膜腔的局部炎症反应:细胞因子,巨噬细胞和其他白细胞对其的调节。

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Studies on infection-induced inflammatory reactions in humans rely largely on findings in the blood compartment. Peritoneal leukocytes from patients treated with peritoneal dialysis offer a unique opportunity to study in humans the inflammatory responses taking place at the site of infection. Compared with peritoneal macrophages (pMϕ) from uninfected patients, pMϕfrom infected patients displayex vivoan upregulation and downregulation of proinflammatory and anti-inflammatory mediators, respectively. Pro-IL-1βprocessing and secretion rather than synthesis proves to be increased in pMϕfrom infectious peritonitis suggesting up-regulation of caspase-1in vivo. A crosstalk between pMϕ,γδT cells, and neutrophils has been found to be involved in augmented TNFαexpression and production during infection. The recent finding in experimental studies that alternatively activated macrophages (Mϕ2) increase by proliferation rather than recruitment may have significant implications for the understanding and treatment of chronic inflammatory conditions such as encapsulating peritoneal sclerosis (EPS).
机译:对人类感染引起的炎症反应的研究主要依赖于血腔中的发现。来自接受腹膜透析治疗的患者的腹膜白细胞提供了一个独特的机会来研究人在感染部位发生的炎症反应。与未感染患者的腹膜巨噬细胞(pMϕ)相比,感染患者的pM display分别表现出体内促炎和抗炎介质的上调和下调。在感染性腹膜炎的pMϕ中,前IL-1β的加工和分泌而非合成被证明增加,表明体内caspase-1的上调。已经发现pM +,γδT细胞和嗜中性粒细胞之间的串扰与感染过程中TNFα的表达和产生增加有关。最近在实验研究中发现,活化的巨噬细胞(Mϕ2)通过增殖而不是通过募集而增加,这可能对理解和治疗慢性炎性疾病(如封装性腹膜硬化(EPS))具有重要意义。

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